A double-strand break repair defect in ATM-deficient cells contributes to radiosensitivity.

@article{Khne2004ADB,
  title={A double-strand break repair defect in ATM-deficient cells contributes to radiosensitivity.},
  author={Martin K{\"u}hne and Enriqueta Riballo and Nicole Rief and Kai Rothkamm and Penny A Jeggo and Markus L{\"o}brich},
  journal={Cancer research},
  year={2004},
  volume={64 2},
  pages={500-8}
}
The ATM protein, which is mutated in individuals with ataxia telangiectasia (AT), is central to cell cycle checkpoint responses initiated by DNA double-strand breaks (DSBs). ATM's role in DSB repair is currently unclear as is the basis underlying the radiosensitivity of AT cells. We applied immunofluorescence detection of gamma-H2AX nuclear foci and pulsed… CONTINUE READING